Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia

Abstract:Altered olfactory function is a common symptom of COVID-19, but its etiology is unknown. A key question is whether SARS-CoV-2 (CoV-2) – the causal agent in COVID-19 – affects olfaction directly, by infecting olfactory sensory neurons or their targets in the olfactory bulb, or indirectly, through perturbation of supporting cells. Here we identify cell types in the olfactory epithelium and olfactory bulb that express SARS-CoV-2 cell entry molecules. Bulk sequencing demonstrated that mouse, non-human primate and human olfactory mucosa expresses two key genes involved in CoV-2 entry, ACE2 and TMPRSS2. However, single cell sequencing revealed that ACE2 is expressed in support cells, stem cells, and perivascular cells, rather than in neurons. Immunostaining confirmed these results and revealed pervasive expression of ACE2 protein in dorsally-located olfactory epithelial sustentacular cells and olfactory bulb pericytes in the mouse. These findings suggest that CoV-2 infection of non-neuronal cell types leads to anosmia and related disturbances in odor perception in COVID-19 patients

Beyond Quantity: Research with Subsymbolic AI

How do artificial neural networks and other forms of artificial intelligence interfere with methods and practices in the sciences? Which interdisciplinary epistemological challenges arise when we think about the use of AI beyond its dependency on big data? Not only the natural sciences, but also the social sciences and the humanities seem to be increasingly affected by current approaches of subsymbolic AI, which master problems of quality (fuzziness, uncertainty) in a hitherto unknown way. But what are the conditions, implications, and effects of these (potential) epistemic transformations and how must research on AI be configured to address them adequately